When lost, look to the heart

6-year-old previously healthy girl arrives by ambulance. Initially somnolent, tachycardic, hypoxic and hypotensive. In the ambulance a peripheral venous line was placed and Ringer acetate set for infusion. During transport, five minutes from the hospital, she suddenly lost consciousness and stopped breathing. Assessed as cardiac arrest CPR was started. Upon arrival there was no palpable pulses or meassurable BP. CPR was continued. ECG showed a narrow complex SVT with a rate of 130 BPM. Hence PEA until echo. Adrenaline was administered, CPR continued. A bolus of 800cc fluid ex-juvantibus was administered without effect. Bedside echo during CPR seen below.

Taking the clinical scenario and echo into account, it was considered reasonable to suspect septic shock and the patient was immediately treated with 1L bolus of fluid due to grave hypovolemia. Furthermore, rapid overview ultrasound shows the following findings in the lateral lung quadrant.

A normal lung ought to beyond the superficial pleura have a black and grey appearance without any organized structures, so called artifacts since the air level can’t reflect the sound waves. In this case we can see organized echogenic consolidations in the lung. Most frequently these changes represent severe pneumonia with empyema or a tumor. Overall assessment was severe hypovolemia secondary to pneumosepsis with shock. The patient responed to the fluid bolus, regained pulse and blood pressure, and was admitted to the intensive care unite for further treatment. She was discharged home 10 days later without any complications.

30 year old man with acute onset chest pain two hours earlier. Radiation to the neck and left arm.

ECG shows ST-elevation V4-V6 with a hint of ST-elevation V2-V3. The morphology leans towards the convex, valley, side. Reciprocal ST depression might be suspected in limb lead III. The patient informs of a fever and diarrhea for the past three days.

Ultrasound of course:

Can you see the regional wall motion abnormality? The inferolateral part of the apex is affected. So how do we proceed? The history and age raises a suspicion of perimyocarditis, but STEMI must be excluded. An emergency percutaneous coronary angiography was performed and showed absolutely fine coronary artery. The first highly sensitive Troponin T 650. In conclusion myocarditis with localized inferolateral RWMA was diagnosed.

See also Amal Mattu’s approach on how to differ myocardial infarction from pericarditis by ECG.

35-year-old woman seeking due to exercise-induced chest pain for three days which has now transitioned into constant pain.

ECG on arrival shows ST depression v4-v6.

Repeat ECG after 15 minutes shows regression of the ST-depressions.

The patient has just performed a stress-ECG!

Can you see the regional wall motion abnormality (RWMA)?

In a stepwise fashion, evaluate each region. As a novice it might be difficult to distinguish RWMA from normal myocardium when looking at the heart as a whole. Feel free placing the mouse pointer over the endocardium to look for dynamic changes in the wall thickness. This is referred to as radial contraction.

Systematic review shows RWMA in the apex and the entire lateral wall.

NSTEMI treatment was instituted. Because of persistent chestpain PCI was performed two hours later showing total occlusion of the LCx.

It was a sunny July afternoon and time to wrap up for the day. A quick glance at the patient list however, and before you knew it I was taking a history.
Intermittent lower leg edema the last couple of months in a 40-or so woman. Physically active every day. No other complaints. No past medical history and no medication. A pinch of short stature and a pinch of overweight. Vital signs were ok. Lower extremities slender. All in all currently asymptomatic and seemingly well. This was a clear-cut case of thoracic aortic aneurysm involving the roots of the coronary arteries. Now all I had to do was convince the surgeon to perform a composite graft implantation.
A quick physical revealed a diastolic decrescendo murmur 2/6 at IC2-3 left parasternal. No rumbling, anterior mitral leaflet Austin-Flynt murmur over the apex, but it was good enough to justify a bedside echo. Lo and behold, a 6cm wide ascending thoracic aortic aneurysm with a mild aortic insufficiency.

But let’s drop the cool. Was this simply an ad-hoc finding? What was I looking for with the ultrasound? To make things clear, a diastolic murmur always warrants further diagnostics. But was the absent lower extremity edema related to the TAA? Perhaps it was, perhaps it wasn’t, perhaps it was hormones. Her neck was a bit short. Webbing of the neck springs to mind, and as such Noonan and Turner syndromes. Just as in Marfan-, Ehler-Danlos- and Loeys-Dietz syndromes, diseases effecting connective tissue, there is a relation to pathology of the aorta. Did I think of this? No. Upon focused history regarding chest pain, burried beneath a thick layer of anxiety, in the trunk of an old caaar, much was revealed. Onset, location, duration, character, alleviating- & aggravating factors, accessory symptom and radiating pain. First onset one year ago, 1-4 times a week, increasing in frequency lately. Episodes described as sudden in onset, retro sternal, stabbing chest pain radiating to the right arm and back. Aggravate by lifting boxes at work or while straining upon defecation, 5-10 minutes of duration, alleviated by rest. Accessory symptom of dispnea while lying supine, alleviated by lying in lateralt decubitus. Compression of adjacent organs? She admitted to rationalizing the pain because there was no radiation to the left arm.

Boy oh boy was I worried. A young, vital woman in her prime with an intermittently symptomatic TAA and open heart surgery around the corner. I’ll leave you suspended in mid-air to appreciate the emotional limbo. Goal systolic BP < 120 until then.